| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Obstetrics and Gynecology, University of Iowa, Iowa City, Iowa, United States
2 Internal Medicine, University of Iowa, Iowa City, Iowa, United States
3 Internal Medicine, University of Iowa, Iowa City, Iowa, United States; Physiology and Biophysics, University of Iowa, Iowa City, Iowa, United States
4 Internal Medicine, University of Iowa, Iowa City, Iowa, United States; VA Medical Center, Iowa City, Iowa, United States
* To whom correspondence should be addressed. E-mail: baoli-yang{at}uiowa.edu.
The present studies were designed to determine if mice heterozygous for
deletion of 
-ENaC exhibited defects in Na+/K+ transport and blood pressure regulation.
In response to an acute KCl infusion +/- mice developed higher serum [K+] and excreted
only 40% of the K+ excreted by +/+ mice. After 6 days on a low (0.01%) Na+ diet, the
cumulative Na+ excretion from day 3-6 was greater for +/- mice. This low Na+ diet
caused higher serum [K+] and lower K+ excretion rates in +/- mice than in +/+ mice, but
the rectal potential differences were not different. Analyses of mRNA from mice on this
diet showed the expected ~50% reduction of -ENaC in kidney and colon of +/- mice.
Unexpectedly, the level of 
-ENaC mRNA was similarly reduced. NHE3 mRNA was
~30% higher in +/- mice while mRNA of the Na/K/2Cl cotransporter was not different.
Also unexpectedly, the amount of -ENaC proteins was similar in both groups of mice
but there was a reduction of one form of -ENaC in +/- mice. These experiments
demonstrate that mice heterozygous for -ENaC have a small but detectable defect in
their ability to conserve Na+ and a more readily apparent defect in the ability to secrete
K+.
This article has been cited by other articles:
|
|
 |
|
  R. Y. Walder, B. Yang, J. B. Stokes, P. A. Kirby, X. Cao, P. Shi, C. C. Searby, R. F. Husted, and V. C. Sheffield Mice defective in Trpm6 show embryonic mortality and neural tube defects Hum. Mol. Genet., November 15, 2009; 18(22): 4367 - 4375. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Spyroglou, J. Manolopoulou, S. Wagner, M. Bidlingmaier, M. Reincke, and F. Beuschlein Short term regulation of aldosterone secretion after stimulation and suppression experiments in mice J. Mol. Endocrinol., May 1, 2009; 42(5): 407 - 413. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 X. R. Cao, N. L. Lill, N. Boase, P. P. Shi, D. R. Croucher, H. Shan, J. Qu, E. M. Sweezer, T. Place, P. A. Kirby, et al. Nedd4 Controls Animal Growth by Regulating IGF-1 Signaling Sci. Signal., September 23, 2008; 1(38): ra5 - ra5. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. P. Shi, X. R. Cao, E. M. Sweezer, T. S. Kinney, N. R. Williams, R. F. Husted, R. Nair, R. M. Weiss, R. A. Williamson, C. D. Sigmund, et al. Salt-sensitive hypertension and cardiac hypertrophy in mice deficient in the ubiquitin ligase Nedd4-2 Am J Physiol Renal Physiol, August 1, 2008; 295(2): F462 - F470. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J Manolopoulou, M Bielohuby, S J Caton, C E Gomez-Sanchez, I Renner-Mueller, E Wolf, U D Lichtenauer, F Beuschlein, A Hoeflich, and M Bidlingmaier A highly sensitive immunofluorometric assay for the measurement of aldosterone in small sample volumes: validation in mouse serum J. Endocrinol., February 1, 2008; 196(2): 215 - 224. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. P. Shi, X. R. Cao, J. Qu, K. A. Volk, P. Kirby, R. A. Williamson, J. B. Stokes, and B. Yang Nephrogenic diabetes insipidus in mice caused by deleting COOH-terminal tail of aquaporin-2 Am J Physiol Renal Physiol, May 1, 2007; 292(5): F1334 - F1344. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
